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Biaxin (Clarithromycin)
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Biaxin

Biaxin is a medication of macrolide antibiotics group. Biaxin fights bacteria in the body. Biaxin is also used together with other medicines to treat stomach ulcers caused by Helicobacter pylori.

Other names for this medication:
Abbotic, Adel, Aeroxina, Althromicin, Apo-clarix, Bacterfin, Biclar, Bicrolid, Binoclar, Biotclarcin, Bremon, Bremon unidia, Ciclinil, Cidoclar, Clabact, Clabel, Clacee, Clacina, Clacine, Clactirel, Clamycin, Clarimac, Clarimax, Clarimed, Clarimycin, Claripen, Clariston, Claritab, Claritron, Claritrox, Claritt, Clariva, Clariwin, Clarix, Clarocin, Clarogen, Claromac, Claromycin, Claron, Clarosip, Claryl, Clarytas, Clasine, Clathrocyn, Clatic, Claxid, Cleanomisin, Cleron, Clonocid, Clormicin, Derizic, Egelif, Eliben, Emimycin, Eracid, Euromicina, Ezumycin, Finasept, Fromilid, Geromycin, Gervaken, Glartin, Hecobac, Heliclar, Helimox, Helozym, Infex, Iset, Italclar, Kailasa, Kalecin, Kalixocin, Karid, Karin, Klabax, Klabet, Klabion, Klarifor, Klarigen, Klariger, Klarimac, Klarimax, Klarit, Klarith, Klarithran, Klarithrin, Klaritpharma, Klax, Klaz, Klazidem, Klerimed, Kleromicin, Klonacid, Kofron, Krobicin, Laricid, Larithro, Larizin, Laromin, Lekoklar, Likmoss, Lyoclar, Macladin, Maclar, Macrobid, Macrol, Macromicina, Mononaxy, Monozeclar, Naxy, Neo-clarosip, Neo-klar, Nexium hp7, Nutabact, Odycin, Onexid, Opeclacine, Orixal, Pre-clar, Preclar, Quedox, Rocin, Rodizim, Rolacin, Rolicytin, Synclar, Taclar, Uniklar, Veclam, Vikrol, Xylar, Zeclar, Zeclaren

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Also known as: Clarithromycin.

Description

Biaxin is used to treat many different types of bacterial infections affecting the skin and respiratory system. Biaxin is also used together with other medicines to treat stomach ulcers caused by Helicobacter pylori.

Biaxin fights bacteria in the body.

Biaxin is also known as Clarithromycin, Maclar, Klaricid, Klacid, Clarimac, Claribid.

Dosage

Biaxin is available in tablets.

Take Biaxin orally.

Take Biaxin with full glass of water.

Take Biaxin with or without food.

Do not crush, chew, or break the Biaxin tablet. Swallow the pill whole.

Shake the Biaxin oral suspension well before measuring a dose. Measure the Biaxin oral suspension with a marked measuring spoon or medicine cup.

Take Biaxin for for 7 to 14 days.

The dosage and the kind of medication depend on the disease and its prescribed treatment.

Do not stop taking Biaxin suddenly.

Overdose

If you overdose Biaxin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Biaxin overdosage: nausea, vomiting, diarrhea, abdominal discomfort.

Storage

Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Protect from light. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Biaxin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Biaxin if you are allergic to its components or to clarithromycin or to similar medicines such as azithromycin (Zithromax), dirithromycin (Dynabac), erythromycin (E.E.S., E-Mycin, Ery-Tab, Erythrocin), troleandomycin (Tao).

Do not take Biaxin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Biaxin if you take astemizole (Hismanal), cisapride (Propulsid), ergot medicine such as ergotamine (Ergomar, Ergostat, Cafergot, Ercaf, Wigraine), or dihydroergotamine (D.H.E. 45, Migranal Nasal Spray), pimozide (Orap), terfenadine (Seldane).

Do not take Biaxin if you have liver disease, kidney disease, myasthenia gravis, porphyria; personal or family history of "Long QT syndrome".

Try to be careful with Biaxin usage in case you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Avoid consuming alcohol.

It can be dangerous to stop Biaxin taking suddenly.

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To determine whether adding simvastatin as adjuvant to triple regimen in patients with H. pylori infection will improve the eradication rate.

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The study took the form of a cost-effectiveness analysis spanning 2 years. The perspective was societal and the setting, ambulatory care. Subjects were Helicobacter pylori-positive patients with a duodenal ulcer. The triple therapy trials spanned 7, 10 or 14 days and the main outcome measures were cost per patient and marginal cost for additional cured patient calculated for a low cost-of-care setting (Spain), for a high-cost setting (USA), and for two follow-up strategies: (i) systematic 13C-urea breath test after eradication; (ii) clinical follow-up, breath-test if symptoms recurred.

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Chronic rhinosinusitis (CRS) is a chronic inflammatory disease of the nasal mucosa. Recent studies suggest that S. aureus enterotoxins may play an etiologic role in the development of CRS. Apart from surgery and repeated courses of steroids, macrolide antibiotics have been reported to exert anti-inflammatory effects in CRS. Similar effects have been reported for fluoroquinolones on various cell types. Since these effects have poorly been characterized in CRS, we examined anti-inflammatory effects of ciprofloxacin on human nasal epithelial cells (HNECs).

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To evaluate the ability of once daily reduced dose clarithromycin to prevent disseminated Mycobacterium avium complex (dMAC) infection in patients with advanced HIV disease.

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Korea and Japan show the highest incidence of gastric cancer and Helicobacter pylori infection. New 2013 guidelines on H. pylori infection differ between the two countries with regard to the indications for H. pylori eradication, diagnostic methods, and treatment regimens. Indications for eradication in Korean guideline focus on specific diseases such as peptic ulcer disease, low-grade gastric mucosa-associated lymphoid tissue lymphoma, and after resection of early gastric cancer, while Japanese guideline includes all H. pylori-associated gastritis for the prevention of dissemination. With regard to the diagnosis, either noninvasive or invasive method (except for bacterial culture) is recommended in Korea, while two noninvasive tests including serum anti-H. pylori IgG antibody level are preferred in Japan. As for the treatment regimens, second-line treatment (quadruple bismuth-containing regimen) is recommended without first-line triple therapy in areas of high clarithromycin resistance in Korea. However, there is no bismuth-based second-line treatment in Japan, and the Japanese regimen consists of a lower dose of antibiotics for a shorter duration (7 days). Such discrepancies between the two countries are based not only on the differences in the literature search and interpretation, but also on the different approvals granted by the national health insurance system, manufacturing process of the antibiotics, and diagnostic techniques in each country. Collaborations are required to minimize the discrepancies between the two countries based on cost-effectiveness.

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A case of fatal pulmonary Mycobacterium abscessus infection in a 56-year-old man is reported. The patient had a longstanding history of seropositive, nodular rheumatoid arthritis with severe joint manifestations that had been treated with a regimen of prednisone, leflunomide, and etanercept. He presented to our facility with complaint of productive cough, persistent fevers, pleuritic chest discomfort, and dyspnea at rest. The patient was admitted to hospital, placed in isolation, a left-sided chest tube was inserted (left pneumothorax identified), and sputum acid-fast bacteria stains and cultures were obtained. Fluorochrome stains demonstrated numerous acid-fast bacteria, and M. abscessus was recovered from the culture media. He was treated with a regimen of amikacin, cefoxitin, and clarithromycin. He initially responded well, and was discharged home with this regimen. He remained afebrile with decreased cough and sputum production until 15 days after discharge when he was again admitted to hospital, with acute onset dyspnea and right-sided chest discomfort (right pneumothorax identified). He ultimately expired, due to overwhelming pulmonary infection, 20 days after readmission to hospital. Autopsy revealed acid fast bacilli in the setting of numerous, bilateral, necrotic, granulomatous, cavitary pulmonary lesions. Based on its mechanism of action, we propose an association between the use of etanercept, a tumor necrosis factor alpha (TNF-alpha) inhibitor, and this case of fatal pulmonary mycobacterial infection. We recommend that physicians exercise cautious clinical judgment when initiating etanercept therapy in persons with underlying lung disease, especially in communities in which mycobacterial organisms are highly prevalent. We also advise physicians to maintain a high level of vigilance for late onset granulomatous infection in persons using etanercept.

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We report on the case of a 9-month-old Caucasian girl referred to our institution with a history of fever of unknown origin and wheezing, unresponsive to bronchodilator and anti-inflammatory therapy. Subsequent investigation led to a diagnosis of mediastinal lymphadenopathy caused by Mycobacterium avium-intracellulare (MAI). The infected lymph tissue infiltrated and obstructed the right bronchus and significantly compressed the left bronchus to the point of near closure. Given the high degree of morbidity and potential mortality from thoracic surgery in this patient, we treated her with a combination of anti-mycobacterial drugs (rifabutin, clarithromycin, ciprofloxacin, clofazimine, amikacin, ethambutol) and glucocorticoids to relieve airway compression. The endobronchial granulation tissue was resected by laser bronchoscopy. This combined approach led to eventual normalization of radiologic and endoscopic findings, and the anti-mycobacterial chemotherapy was discontinued 12 months after the first bronchoalveolar lavage culture was negative for MAI. The patient remains asymptomatic 1 year after completion of this course of therapy. We suggest that mediastinal lymphadenopathy with bronchial infiltration and extrinsic airway compression caused by MAI in otherwise healthy children can be successfully treated with aggressive chemotherapy, glucocorticoids, and laser bronchoscopy.

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CD30+ cutaneous lymphoproliferative disorders (CLPDs) are usually characterized by a benign clinical course. The prognostic value of cytotoxic markers in these lymphomas has not been evaluated in large series. We describe a case of borderline CD30+ CLPD with cytotoxic phenotype, presenting in a 22-year-old male patient as an ulcer on the forearm. He reported having had similar ulcers on the buttock and thigh that spontaneously regressed over the course of 1 year. The lesion resolved with a single course of clarithromycin; a subsequent lesion, too, responded to clarithromycin, and no recurrences or systemic involvement have been documented in the 9-month follow-up. A conservative approach in the management of CD30+ CLPD is recommended. We believe that the anti-inflammatory and apoptotic effects of clarithromycin on T cells may have hastened the remission process.

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Clarithromycin has bacteriologic efficacy against M avium infection in late-stage AIDS, although drug resistance eventually develops. Further studies are needed to investigate safe, effective concomitant drugs.

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In vitro studies have demonstrated that formation of reactive oxygen species (ROS) contributes to the effect of bactericidal antibiotics. The formation of ROS is not restricted to bacteria, but also occurs in mammalian cells. Oxidative stress is linked to several diseases. This study investigates whether antibiotic drugs induce oxidative stress in healthy humans as a possible mechanism for adverse reactions to the antibiotic drugs.

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Sixty-three cases of M marinum infection were studied. In 53 (84%) of Combivir Cost the patients, inoculation was related to fish tank exposure. The site of infection was mainly the upper limb (in 60 [95%] of the 63 patients), and infection was spread to deeper structures in 18 (29%) of the patients. All patients were treated with antibiotics (median time, 3(1/2) months), and 30 (48%) underwent surgery. Various antibiotic regimens were prescribed, and the initial regimen was modified in 22 (35%) of the patients. Clarithromycin, cyclines, and rifampin were the most commonly prescribed antibiotics. Cure was observed for 55 (87%) of the patients. Failure was related to deep structure involvement (3 of 45 vs 5 of 18 patients; P =.04) but not to any antibiotic regimen. All strains showed the same susceptibility pattern without acquired resistance. The 90% minimum inhibitory concentrations of rifampin and rifabutin were far lower (0.5 and 0.06 micro g/mL, respectively) than the 90% minimum inhibitory concentrations of clarithromycin (2 micro g/mL) and the cyclines (minocycline, 4 micro g/mL; and doxycycline, 8 micro g/mL).

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The in-vitro effects of ten antimicrobial agents on the biofilm formation of Pseudomonas aeruginosa were investigated. The production of alginic acid by mucoid P. aeruginosa cells cultured in agar media with sub-MICs of antimicrobial agents was quantified by high-performance liquid chromatography. Alginic acid production was inhibited by 1/4 MIC of minocycline (P < 0.002) and tobramycin (P < 0.02), and by 1/256-1/1/64 MIC of macrolides (erythromycin, clarithromycin, roxithromycin, and rokitamycin) and clindamycin (P < 0.02), compared with drug-free controls. Piperacillin, ceftazidime, and ofloxacin did not inhibit alginic acid production. The production of exopolysaccharide by non-mucoid P. aeruginosa cells grown on silicone plates in sub-MICs of antimicrobial agents was determined by quantitative tryptophan assay. Exopolysaccharide production was inhibited by 1/16 MIC of macrolides and clindamycin, but not by other antimicrobial agents. Electron microscopy showed that biofilm formation by mucoid and non-mucoid type P. aeruginosa strains was inhibited by sub-MICs of Zithromax Online Overnight erythromycin and correlated with the in-vitro production of alginic acid and exopolysaccharide. These results suggest that sub-MICs of macrolides and clindamycin suppress biofilm formation by P. aeruginosa and that intractable chronic respiratory tract infections due to P. aeruginosa might be prevented.

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We studied the comparative in vitro activities of ABT-773, a new ketolide, against 268 aerobic and 148 anaerobic recent isolates from clinical bites using an agar dilution method and inocula of 10(4) CFU/spot for aerobes and 10(5) CFU for anaerobes. The following are the MIC ranges and MICs at which 90% of isolates are inhibited (MIC(90)s) of ABT-773 for various isolates, respectively: Pasteurella multocida and Pasteurella septica, 0.125 to 2 and 1 microg/ml; other Pasteurella species, 0.125 Imodium Online to 1 and 0.5 microg/ml; Corynebacterium spp., 0.015 to 0.06 and 0.015 microg/ml; Staphylococcus aureus, 0.03 to 0.06 and 0.06 microg/ml; coagulase-negative staphylococci, 0.015 to >32 and 32 microg/ml; streptococci, 0.015 to 0.03 and 0.03 microg/ml; Eikenella corrodens, 0.25 to 1 and 1 microg/ml; and Bergeyella zoohelcum, 0.03 to 0.25 and 0.06 microg/ml. For anaerobes the MIC ranges and MIC(90)s of ABT-773 were as follows, respectively: Prevotella heparinolytica, 0. 06 to 0.125 and 0.125 microg/ml; Prevotella spp., 0.015 to 0.125 and 0.06 microg/ml; Porphyromonas spp., 0.015 to 0.03 and 0.015 microg/ml; Fusobacterium nucleatum, 0.5 to 8 and 8 microg/ml; other Fusobacterium spp., 0.015 to 8 and 0.5 microg/ml; Bacteroides tectum, 0.015 to 0.5 and 0.06 microg/ml; and Peptostreptococcus spp., 0.015 to 0.25 and 0.03 microg/ml. ABT-773 was more active than all macrolides tested against S. aureus, E. corrodens, and anaerobes, but all compounds were poorly active against F. nucleatum. The activity of ABT-773 was within 1 dilution of that of azithromycin against Pasteurella spp., and ABT-773 was four- to eightfold more active than clarithromycin against Pasteurella spp. ABT-773 may offer a therapeutic alternative for bite wound infections.

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At week Sinequan Generic 8, baseline UAS reduced from 4.7 +/- 1.1 to 2.4 +/- 1.4 (p = .027) in group A and from 4.3 +/- 1.5 to 2.3 +/- 1.2 (p = .008) in group B, without statistically significant difference between the two groups. In control group and in six patients with H. pylori eradication failure, no changes of UAS were noted.

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The eradication rates for rabeprazole-amoxicillin-metronidazole were 88% (81/92) using intention Buy Grifulvin Online -to-treat analysis and 91% (81/89) using per protocol analysis. The eradication rates were 97% (61/63) for metronidazole-sensitive strains and 82% (18/22) for metronidazole-resistant strains.

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Now that treatment of H. pylori associated disease is becoming common in Japan, drug resistant--H. pylori has emerged as a problem to be solved. There is no standard method of H. pylori drug susceptibility test in Japan yet. There are several methods available: Disk test, E-test, microplate method and agar plate dilution method. The E-test is being the standard method in European countries and USA. However the microplate method has been reported as a same accuracy as the agar dilution method, and thought as being a new standard method in Japan. In 2000, The Japanese Society Aricept Generic Costco of Chemotherapy proposed that drug susceptibility test be standardized and listed the break point of MIC of amoxicillin(AMPC) and clarithromycin(CAM).

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Trials were selected if they met the following Vytorin Generic Cost criteria: design - random allocation of participants; participants - anyone with cancer receiving chemotherapy or radiotherapy treatment for cancer; interventions - agents prescribed to prevent oral mucositis; outcomes - prevention of mucositis, pain, amount of analgesia, dysphagia, systemic infection, length of hospitalisation, cost and patient quality of life.

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A prospective study of the clinical efficacy of an aminoglycoside antibiotic (streptomycin, SM) for the treatment of pulmonary Mycobacterium avium complex (MAC) disease was carried out. In a multicenter trial, patients with pulmonary MAC disease received protocol-guided combined chemotherapy with or without SM. SM was given to the patients intramuscularly 15 mg/kg three times per week for the initial 3 months and three other antibiotics (rifampicin, ethambutol, and clarithromycin) were added and administered for over 24 months after the conversion of MAC strains. From April 1998 to December 2004, 160 HIV-negative patients were enrolled in this trial. Fourteen patients were found to be ineligible because they could not continue the treatment, and they were excluded from the Trileptal Vs Generic analysis after randomization. Seventy-three patients were assigned to receive combined chemotherapy with SM (group A) and 73 were assigned to receive combined chemotherapy without SM (group B). The median durations of treatment were 27.6 months in group A and 28.4 months in group B. The difference in the backgrounds of the groups was not statistically significant. There were no differences in microbiological and radiological findings between the groups, but the sputum conversion rate for pulmonary MAC disease at the completion of treatment was significantly higher in group A than that in group B. Although, there were no significant differences in the sputum relapse rate and clinical improvement including both clinical symptoms and radiological findings, group A showed better initial microbiological response than group B. As for adverse reactions and abnormal laboratory findings, there were no significant differences between the groups. Based on the results of this double-blind randomized study, we support treatment including SM according to both the American Thoracic Society (ATS) and the Japanese Society for Tuberculosis (JST) guidelines for patients with pulmonary MAC disease without HIV infection.

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Resistance of Haemophilus influenzae from clinical isolates can be predicted on the basis of results of antimicrobial susceptibility of nasopharyngeal isolates. The carriage rate and the antimicrobial susceptibility of H. influenzae isolated in healthy children attending day-care centres in Moscow, Smolensk and Yartsevo was studied. The susceptibility of ampicillin, amoxycillin/clavulanate, cefaclor, erythromycin, roxithromycin, clarithromycin and trimethoprim-sulphamethoxazole were determined by the E-test. The mean carriage rate of H. influenzae was 44%. Resistance of H. influenzae to ampicillin was 2.3%, to amoxycillin/clavulanate 0.7%, to cefaclor 0.7%, to clarithromycin 18.7% and to trimethoprim-sulphamethoxazole 21%. These included strains that showed intermediate-resistance. The antimicrobial resistance profiles varied in different centres. The clinical use of trimethoprim-sulphamethoxazole should be restricted because of the high resistance of H. influenzae to antifolate compounds.

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The intracellular activities of clarithromycin and erythromycin, alone and in combination with other antimicrobial agents, were tested against Mycobacterium avium complex (MAC) strains inside mouse J774 cells and inside alveolar macrophages obtained from human immunodeficiency type 1-infected individuals. Clarithromycin alone had greater intracellular activity than erythromycin alone, and drug combinations that included clarithromycin were usually more active than combinations that included erythromycin.